Circulation Research. 2001;89:273-278
Published online before print July 19, 2001, doi: 10.1161/hh1501.094266
Published online before print July 19, 2001, doi: 10.1161/hh1501.094266
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© 2001 American Heart Association, Inc.
Integrative Physiology |
Acetylcholine, Bradykinin, Opioids, and Phenylephrine, but not Adenosine, Trigger Preconditioning by Generating Free Radicals and Opening Mitochondrial KATP Channels
From the Departments of Physiology (M.V.C., X.-M.Y., G.S.L., G.H., J.M.D.) and Medicine (M.V.C.), College of Medicine, University of South Alabama, Mobile, Alabama, and Department of Pathophysiology (G.H.), University of Essen Medical School, Essen, Germany.
Correspondence to Michael V. Cohen, MD, Department of Physiology, MSB 3050, College of Medicine, University of South Alabama, Mobile, AL 36688-0002. E-mail mcohen{at}usamail.usouthal.edu
Abstract— It has been assumed that all Gi-coupled receptors trigger the protective action of preconditioning by means of an identical intracellular signaling pathway. To test this assumption, rabbit hearts were isolated and perfused with Krebs buffer. All hearts were subjected to a 30-minute coronary artery occlusion followed by 120 minutes of reperfusion. Risk area was measured with fluorescent particles and infarct size with triphenyltetrazolium chloride staining. Control hearts showed 29.1±2.8% infarction of the risk zone. A 5-minute infusion of acetylcholine (0.55 mmol/L) beginning 15 minutes before the 30-minute occlusion resulted in significant protection (9.2±2.7% infarction). This protection could be blocked by administration of 300 µmol/L N-2-mercaptopropionyl glycine (MPG), a free radical scavenger, or by 200 µmol/L 5-hydroxydecanoate (5-HD), a mitochondrial KATP antagonist, for 15 minutes beginning 5 minutes before the acetylcholine infusion (35.2±3.9% and 27.8±2.4% infarction, respectively). Similar protection was observed with other known triggers, ie, bradykinin (0.4 µmol/L), morphine (0.3 µmol/L), and phenylephrine (0.1 µmol/L), and in each case protection was completely abrogated by either MPG or 5-HD. In contrast, protection by adenosine or its analog N6-(2-phenylisopropyl) adenosine could not be blocked by either MPG or 5-HD. Therefore, whereas most of the tested agonists trigger protection by a pathway that requires opening of mitochondrial KATP channels and production of free radicals, the protective action of adenosine is not dependent on either of these steps. Hence, it cannot be assumed that all Gi-coupled receptors use the same signal transduction pathways to trigger preconditioning.
Key Words: acetylcholine • adenosine • free radicals • KATP channels • preconditioning
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